RENAL POTASSIUM SECRETION INCREASES DURING HEMORRHAGE IN A RAT MODEL OF HEMORRHAGIC SHOCK
Debby Lee1, Claudia A Hernandez2, Aileen K Sato2, Lee-Ann M Murata2, Catherine F T Uyehara2.
1University of California, Merced, Merced, CA, 2Tripler Army Medical Center, Honolulu, HI.
Trauma is the leading cause of death in young adults worldwide, and up to 50% of these deaths involve hemorrhage. Hyperkalemia has been reported to be associated with non-survival of severe hemorrhage. During shock, urine flow is dramatically decreased, and thus, in order to maintain electrolyte balance, renal handling of solute secretion must be altered. In this study, we tested the hypothesis that the kidneys respond to hemorrhage by increasing potassium (K) secretion to prevent hyperkalemia. To elucidate the acute effects of hemorrhage on renal electrolyte regulation, we compared renal handling of K and sodium (Na) in conscious, chronically-catheterized rats (n = 4) before, during, and after hemorrhage (2 ml shed blood/100 g body weight (BW)). After 1 hour of sustained hypotension, rats were resuscitated with normal saline. With shock, urine flow dramatically decreased (15 ± 5 to 4 ± 1 ul/min/100g BW) between baseline and hemorrhage periods, and Na clearance also concomitantly decreased (14 ± 4 to 3 ± 1 ul/min/100g). In contrast, we discovered that K clearance was maintained and urine K levels increased (103 ± 22 to 177 ± 25 mmol/L). There was an increase in the trans-tubular K gradient (10 ± 0.5 to 14 ± 1) suggesting a relative increase in renal tubular potassium secretion. Thus, increased tubular K secretion appears to play an important role in the regulation of K homeostasis during hemorrhage. This increase in K secretion may protect against hyperkalemia in hemorrhagic shock.